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Acute myocarditis mimicking lateral myocardial infarction.

SUMMARY

We report a case of myocarditis mimicking acute lateral myocardial infarction and treated as such initially, which was complicated by ventricular fibrillation a few hours after admission to the intensive care unit. The correct diagnosis was rapidly made using a low-dose delayed-enhanced cardiac multidetector computed tomography scan performed immediately after a normal coronary angiogram, demonstrating typical myocardial late hyperenhancement and good correlation with delayed enhanced magnetic resonance imaging. This case suggests that myocarditis can be accurately diagnosed by delayed-enhanced cardiac multidetector computed tomography in an emergency setting. The other lesson from this case is that patients presenting with severe clinical symptoms, important ECG signs and high myocardial enzyme levels should be closely monitored for at least 72 hours, even when myocardial infarction has been excluded.

Key Words: myocarditis, myocardial infarction, coronary angiography, computed tomography, delayed-enhanced computed tomography

CASE HISTORY

A 23-year-old male farmer with no cardiovascular risk factors and no personal or familial record of cardiovascular disease was referred to our intensive care unit with the diagnosis of acute lateral ST-elevated myocardial infarction.

This patient had presented with increasing chest pain for 24 hours, secondarily associated with shortness of breath. No recent infectious episode was reported initially. As chest pain increased, he called for the emergency doctors (Medical Intensive Care Unit). The initial ECG on site showed significant ST-elevation on all lateral leads, so the patient received pre-hospital thrombolysis (tenecteplase) with a loading dose of aspirin and clopidogrel and was immediately transfered to our cardiac catheter laboratory.

Coronary angiography did not show any significant coronary occlusion or stenosis and was considered normal.

Five minutes after coronary angiography, a low-dose cardiac multidetector computed tomography scan was peformed on a Brilliance 64 scanner (Philips Medical Systems, Best, The Netherlands) using retrospective ECG-gating. The parameters of acquisition were as follows: number of detectors, 64; individual detector width, 0.625 mm; gantry rotation time, 420 ms; imaging direction, craniocaudal; pitch, 0.2; half scan reconstruction. Tube current was fixed at 80 kV and 600 mA. Reconstruction parameters for axial slices were 2 mm effective section thickness, 1 mm increment, standard intermediate reconstruction filter (kernel CB) and adapted field of view. Retrospective reconstruction in the mid-diastolic phase (75% of the R-R interval) was performed. This delayed acquisition was performed without any additional injection of contrast medium other than that used for coronary angiography (50 ml of Iomeron 400, Bracco, Milan, Italy).

Delayed-enhanced cardiac multidetector computed tomography scan (DE-MDCT) acquisition showed late hyperenhancement of the lateral myocardial wall with a predominant sub-epicardial distribution (Figure 1). Abnormal myocardial enhancement appeared as nodular bright areas within the left ventricular wall.

Chest pain resolved progressively with aspirin and analgesics. Trans-thoracic echocardiography showed a sub-normal left ventricular ejection fraction (LVEF) of 58% with no left ventricular dilation and discrete segmental hypokinesia of the lateral wall. There was no pericardial effusion.

Heart rhythm was irregular with frequent monomorphic ventricular extrasystoles. About 15 hours after admission and at rest, the patient suffered an episode of ventricular fibrillation. Sinus rhythm was restored by a shock of 150 J. Immediate anti-arrhythmic therapy was started intravenously with magnesium and amiodarone associated with oral beta-blockers.

[FIGURE 1 OMITTED]

Haematological investigations showed a moderate inflammatory syndrome with a C-reactive protein at 14 mg/l and a normal white blood cell count, a troponin-I peak at 81 [micro]g/l (normal value <0.1 [micro]g/l) and a creatine kinase peak of 2500 UI/l (normal value <120 UI/l). All serologic viral tests were negative.

A cardiac magnetic resonance study with intravenous injection of gadolinium was performed 72 hours after admission, confirming normal global systolic function and normal volumetric and ventricular mass values. Breath-hold T2 weighted acquisitions were acquired before contrast injection showing myocardial oedema predominant in the infero-lateral wall (Figure 2). There was also a late gadolinium enhancement of the subepicardial lateral wall (Figure 3), thus confirming the diagnosis of acute myocarditis. There was good correlation between DE-MDCT and delayed-enhanced MRI images (DE-MRI).

After 72 hours of surveillance in the intensive care unit, the patient was transferred to a medical unit. After a further four days surveillance in a medical unit without any clinical events, the patient was discharged home on beta-blockers and angiotensin-converting enzyme inhibitors. The medical follow-up at four months was uneventful.

[FIGURE 2 OMITTED]

[FIGURE 3 OMITTED]

DISCUSSION

This case illustrates acute myocarditis complicated by ventricular fibrillation but with a clinical presentation mimicking acute lateral myocardial infarction. It was accurately diagnosed by DE-MDCT immediately following coronary angiography.

The accuracy of DE-MDCT compared with DE-MRI for the diagnosis of acute myocarditis has been assessed in two small series of patients with a significant correlation between both methods (1,2). As for DE-MRI, DE-MDCT allows differentiation between acute myocarditis and myocardial infarction in patients with acute chest pain consistent with myocardial ischaemia. The accuracy of DE-MDCT has been studied more in the acute setting of myocardial infarction in experimental (3,4) and clinical studies (5,6) and segmental analysis revealed good agreement with DE-MRI for both involved/healthy segments classification and transmural extent of myocardial enhancement.

This is the first reported case to show that DE-MDCT performed directly after coronary angiography without the need of another iodinate contrast injection can yield good results compared to DE-MRI performed three days later. All previous studies assessed DE-MDCT after an 80 to 100 ml intravenous injection of iodinate contrast. Performing the CT scan directly after a normal coronary angiogram not only allows an accurate diagnosis of the underlying myocardial disease but also avoids another injection of nephrotoxic contrast media and diminishes the overall quantity of injected drugs. However, this protocol of investigation needs to be evaluated by further studies.

Although DE-MRI provides an accurate assessment of the site and activity of myocardial inflammation and improves the accuracy of endomyocardial biopsies for the diagnosis and viral aetiology assessment of myocarditis (7-9), its availability in an emergency setting is a limitation compared to MDCT. In the differential diagnosis of acute chest pain in potentially unstable patients, contrast-enhanced MDCT can accurately assess coronary arteries, providing differential diagnosis with aortic dissection or pulmonary embolism (10). As such, DE-MDCT might be considered as a first-line imaging modality in patients with a strong clinical suspicion of acute myocarditis but in which ECG modifications suggest a possible acute myocardial infarction.

Another striking aspect of this case report was the recorded episode of ventricular fibrillation occurring at rest and a few hours after admission.

Ventricular arrythmias occuring in the setting of acute myocarditis have been described in the literature and myocarditis is one of the leading causes of sudden deaths in chidren and young adults, responsible for 20 to 40% of them (11). Numerous factors contribute to the development of ventricular arryhthmias in myocarditis such as myocardial inflammation, myocardial damage, ischaemic events due to vasculitis or microvascular dysfunction and ventricular fibrosis with LVEF alterations (9,11,12). Yet the clinical course of patients with myocarditis remains poorly defined and there are no pertinent criteria to predict the occurrence of malignant ventricular arrhythmias in such patients.

The incidence of ventricular arrhythmias in myocarditis is not precisely known even though the final outcome seems to be favourable in most cases. Arrhythmic evaluation by 24 h Holter ECG, measurement of ventricular late potentials and heart rate variability have been suggested for risk stratification and programmed ventricular electrophysiological stimulation has a relatively high predictive value for spontaneous ventricular tachyarrhythmias in selected groups of patients with myocarditis (12). Unfortunately, at the present time optimal electrophysiological parameters with a high predictive value do not exist. The same can be said about the therapeutic management of such patients with antiarrythmic drugs which remains to be assessed by future prospective studies.

In summary, the presented case suggests that myocarditis can be accurately diagnosed by DE-MDCT in an emergency setting immediately after coronary angiography or even at first hand. The other lesson from this case is that patients presenting with severe clinical symptoms, important ECG signs and high myocardial enzyme levels should be closely monitored for at least 72 hours, even when myocardial infarction has been excluded.

Accepted for publication on June 17, 2008.

REFERENCES

(1.) Boussel L, Gamondes D, Staat P, Elicker BM, Revel D, Douek P. Acute chest pain with normal coronary angiogram: role of contrast-enhanced multidetector computed tomography in the differential diagnosis between myocarditis and myocardial infarction. J Comput Assist Tomogr 2008; 32:228-232.

(2.) Dambrin G, Laissy JP, Serfaty JM, Caussin C, Lancelin B, Paul JF. Diagnostic value of ECG-gated multidetector computed tomography in the early phase of suspected acute myocarditis. A preliminary comparative study with cardiac MRI. Eur Radiol 2007; 17:331-338.

(3.) Lardo AC, Cordeiro MA, Silva C, Amado LC, George RT, Saliaris AP et al. Contrast-enhanced multidetector computed tomography viability imaging after myocardial infarction: characterization of myocyte death, microvascular obstruction, and chronic scar. Circulation 2006; 113:394-404.

(4.) Baks T, Cademartiri F, Moelker AD, Weustink AC, van Geuns RJ, Mollet NR et al. Multislice computed tomography and magnetic resonance imaging for the assessment of reperfused acute myocardial infarction. J Am Coll Cardiol 2006; 48:144-152.

(5.) Ko SM, Seo JB, Hong MK, Do KH, Lee SH, Lee JS et al. Myocardial enhancement pattern in patients with acute myocardial infarction on two-phase contrast-enhanced ECG-gated multidetector-row computed tomography. Clin Radiol 2006; 61:417-422.

(6.) Paul JF, Wartski M, Caussin C, Sigal-Cinqualbre A, Lancelin B, Angel C et al. Late defect on delayed contrast-enhanced multidetector row CT scans in the prediction of SPECT infarct size after reperfused acute myocardial infarction: initial experience. Radiology 2005; 236:485-489.

(7.) Laissy JP, Hyafil F, Feldman LJ, Juliard JM, Schouman-Claeys E, Steg PG et al. Differentiating acute myocardial infarction from myocarditis: diagnostic value of early- and delayed-perfusion cardiac MR imaging. Radiology 2005; 237:75-82.

(8.) Mahrholdt H, Goedecke C, Wagner A, Meinhardt G, Athanasiadis A, Vogelsberg H et al. Cardiovascular magnetic resonance assessment of human myocarditis: a comparison to histology and molecular pathology. Circulation 2004; 109: 1250-1258.

(9.) Mahrholdt H, wagner A, Deluigi CC, Kispert E, Hager S, Meinhardt G et al. Presentation, patterns of myocardial damage, and clinical course of viral myocarditis. Circulation 2006; 114:1581-1590.

(10.) Johnson TR, Nikolaou K, Wintersperger BJ, Knez A, Boekstegers P, Reiser MF et al. ECG-gated 64-MDCT angiography in the differential diagnosis of acute chest pain. AJR Am J Roentgenol 2007; 188:76-82.

(11.) Feldman AM, McNamara D. Myocarditis. N Engl J Med 2000; 343:1388-1398.

(12.) Klein RM, Vester EG, Brehm Mu, Dees H, Picard F, Niederacher D et al. [Inflammation of the myocardium as an arrhythmia trigger]. Z Kardiol 2000; 89 (Suppl 3):24-35.

N. MOTTARD *, N. MEWTON ([dagger]), E. BONNEFOY ([double dagger]), M. ABDELLAOUI *, D. REVEL ([sections]), G. KIRKORIAN **

Intensive Care Unit, Hopital Cardiologique Louis Pradel, Lyon, France

* M.D., Fellow.

([dagger]) M.D., Cardiologist.

([double dagger]) M.D., Ph.D., Permanent Doctor.

([sections]) M.D., Chief of Staff, Radiologist, Department of Radiology.

** M.D., Chief of Staff.

Address for reprints: Dr N. Mewton, Unite 51, Service du Pr Kirkorian, Hopital Cardiovasculaire Louis Pradel, 28 avenue Doyen Lepine, 69500 Bron, France.
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Article Details
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Author:Mottard, N.; Mewton, N.; Bonnefoy, E.; Abdellaoui, M.; Revel, D.; Kirkorian, G.
Publication:Anaesthesia and Intensive Care
Article Type:Case study
Geographic Code:4EUFR
Date:Sep 1, 2008
Words:1838
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